What causes nephrocalcinosis and urolithiasis in hyperchloremic acidosis?

Updated: Oct 18, 2018
  • Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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An important complication of chronic renal tubular acidosis (mainly distal, type I) is nephrocalcinosis and urolithiasis. A number of pathophysiological alterations contribute to stone formation:

  • Buffering of the chronic acid load by the bone, causing bone dissolution and promoting hypercalciuria

  • Diminution of renal tubular calcium reabsorption, further aggravating the hypercalciuria

  • Hypocitraturia because of avid citrate reabsorption by the PCT

  • High urinary pH, causing insolubility of calcium phosphate and promoting its precipitation

In contrast, stone disease is rare with type II RTA because of the difference in its pathogenesis. Since the fall in plasma HCO3- is nonprogressive, after the renal HCO3 threshold is reached (transport maximum not exceeded), there is complete absorption of luminal HCO3. At this point, the urine pH is acid, since urine is devoid of HCO3- and there is no defect in distal proton secretion. The daily acid load is thus excreted by the collecting duct, obviating the need for bone buffering. Also, citrate usually escapes proximal reabsorption (along with other solutes) and promotes calcium phosphate solubility.

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